期刊
EXPERIMENTAL BRAIN RESEARCH
卷 214, 期 4, 页码 503-513出版社
SPRINGER
DOI: 10.1007/s00221-011-2849-y
关键词
Cerebral ischemia; Whisker stimulation; Neurovascular unit; VEGF/VEGFR2 signaling; Semaxinib
资金
- NIH [NS 045810, NS062097, NS058710, NS057255]
- American Heart Association
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
Ischemic stroke is a major cause of mortality and morbidity worldwide but effective treatments are limited. Strategies to enhance neurovascular remodeling following stroke provide promising opportunities to improve tissue repair and functional recovery. We have previously demonstrated that whisker activity promotes central angiogenesis in rodent models of whisker-barrel cortex stroke. However, the mechanisms involved in the regulation of neurovascular plasticity by peripheral stimulation are not well-defined. Here, we report that angiogenesis and neurogenesis occur concurrently after cerebral ischemia and whisker stimulation in mice. We show that neuroblasts expressing vascular endothelial growth factor receptor 2 (VEGFR2) migrate along the vessels. Blocking VEGFR2 with the selective inhibitor SU5416 (semaxinib) attenuates ischemia-induced regenerative responses and completely prevents whisker stimulation-induced neurovascular remodeling. These results suggest that VEGFR2-mediated signaling plays an important role in promoting post-ischemia neurovascular remodeling and provides a link between angiogenesis and neurogenesis.
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